Mechanical inspiration (positive pressure lung inflation), conventionally applied to patients with acute cardio-respiratory failure, distends the lungs, increases airway pressure, and produces an increase in mean intrathoracic pressure. However, the benefit derived by the patient from this increase in functional lung volume is actually offset by the increase in intrathoracic pressure, since the latter produces a decrease in venous return to the heart, a decrease in transmural right atrial pressure (right ventricular filling pressure) and limits right ventricular stroke output. Because the pulmonary circulation serves as a conduit from the right ventricle to the left ventricle and has a high capacitance relative to the right heart, transmural left atrial pressure (left ventricular filling pressure) and left ventricular stroke output are similarly decreased. There is a 2-5 beat phasic delay of this effect relative to the right heart. This is the primary mechanism of decreased cardiac output in all patients during mechanical ventilation in which positive pressure lung inflation is applied either continuously (CPPV) or intermittently (IMV).
In general, cardiac output may be reduced by 50-75% during mechanical ventilation, which may have profound effects on organ blood flow, tissue perfusion, and patient survival. Further, declines in cardiac output will be accentuated in settings of functional hypovolemia, myocardial ischemia and infarction, decreased vasomotor tone, large tidal volume breathing, prolonged inspiratory time, and the application of positive end-expiratory pressure (ubiquitously applied to patients with acute respiratory failure to maintain oxygenation and pulmonary gas exchange).
Changes in aortic pulse pressure and mean arterial blood pressure can also occur during positive pressure inspiration. For example, peak positive pressure inspiration produces a net increase in the series resistance of the pulmonary circulation. Because the pulmonary circulation mechanically couples right and left heart output, an increase in pulmonary vascular resistance, such as that which occurs with conventional low rate, high volume mechanical ventilation (i.e., CPPV, IMV), will impede right ventricular ejection and increase right ventricular dimension and wall stress to produce myocardial ischemia. Decreased right ventricular ejection will decelerate pulmonary blood flow and decrease the filling of the left ventricle, establishing a condition of right and left ventricular interference. This results in decreased left heart preload (decreased left ventricular filling due to left ventricular volume encroachment by the overdistended right ventricle) and decreased left heart ejection. In this way, conventional mechanical ventilation may produce profound cardiocirculatory dysfunction by altering both the series and parallel relationships of right and left ventricular function.
There have been some attempts to alleviate the adverse effects of mechanical inspiration on circulation by momentarily decreasing the pressure of the respiration gas with the aid of a pulse-synchronized signal during the propagation time of the pulse wave in the alveolar flow path, and then immediately re-establishing the pressure that existed prior to the decrease. Proper synchronization of pulses assists in filling of the left atrium of the heart. This is somewhat beneficial, but does not deal with the overall problem of decreased biventricular preload secondary to increased mean intrathoracic pressure.